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 I.

DEFINITION: Neoplasia means “new growth”

and the new growth is “NEOPLASM”.
 The term tumor was originally applied to the
swelling caused by inflammation.
 The term tumor now equated with
 Neoplasma is an abnormal mass of tissue, the
growth of which exceeds and is
uncoordinated with that of the normal tissue
and persists in the same excessive manner
after cessation of the stimuli which evoked.
 All tumors benign & malignant, have two
basic component:
1.Proliferating neoplastic cells that constitute
their parenchyma.
2.Suporting stroma made up of connective
tissue and blood vessel.

In general these are designated by attachyng
the suffic “oma” to the cell origin.
 From fibroblastic cells called fibroma.
 From cartilaginous tumor is a chondroma.
 From osteoblast is an osteoma.
 Adenoma that form glandular patern.
 Papiloma: macroscopy & microscopically
visible finger like.
 Cystadenoma: those that form cyctic masses.
 Polyp: when neoplasm benign or malignant
produces a macroscopy visible projection
above a mucosal surface and projects.
 Malignant tumors arising in mesenchymal
tissue are usually called SARCOMA.
 E.g: Fibrosarcoma, Liposarcoma,
Leiomyosarcoma, Rhabdomyosarcoma.

 Malignant neoplasma of epithelial cell origin,

derived from any of the three germ layers are
 E.g: Squamous cell carcinoma,
Adenocarcinoma, Basal cell carcinoma.
 In frequently divergent differentiantion of
single line of parenchymal cell creates what
 E.g: Mixed tumor of salivary gland origin.
 Teratoma is made up of a variety of
parenchymal cell types representative of
more than one germ layer, usually all three.
 E.g: Ovarian cystic teratoma (Dermoid cyst).
 An ectopic rest of normal tissue.
 E.g: a pancreas nodular rest in the mucosa of
small intestine.
 Abberant differentiation may produced a
mass of disorganized but mature specialized
cells or tissue indigenous to the partial site:
 A. Differentiation & Anaplasia.
 Differentiation refer to the extent to which
parenchymal cell resemble comparable
normal cell, both morphologically and

 Anaplasia mean “to form backward” implying

a reversion from a high level of diferentiation
to a lower level.
 Anaplasia is marked by a number of
morphologic and functional change.
Both the cells and nuclei characteristically
 -Pleomorphism: variation in size and shape.
 -Hyperchromatic: the nuclei contain an
abundance of DNA and are extremely dark
 -Large nucleoli are usually present in these
-Large number of atypical mitosis.
-Formation of giants cell tumor.
-N/C ratio (nucleus, cytoplasma). Near 1:1,
Normal 1:4 or 1:6.

Most benign tumors grow slowly over a
period of years, where as most cancers grow
 In general the growth rate of tumors
correlates with their level of diferentiation
and thus most malignant tumor growth more
rapidly than do benign lesion.

Nearly all benign tumors grow as cohessive
expansile masses that remain to their site of
origin and do not have the capacity to
infiltrate, invade or metastasis to distant sites
 Usually develop a rim of compressed
connedted tissue, some time called a fibrous

 The growth of cancers is accompanied by

progressive infiltration, invasion &
destruction of the surrounding tissue.
Metastasis unequivocally marks a tumor as
malignant, because benign neoplasms do not

 Path ways of spread.

1.Seeding of body cavities and surface.
E.g: carcinoma arising in the ovaries.
2.Lymphatic spread:
E.g: carcinoma of the breast.
 3.Hematogenous spread.
This pathway is typical of sarcoma but is also
used by carcinoma.
 Grading of a cancer is based on the degree of
differentiation of the tumor cells and number
of mitosis within the tumor as presummed
correlates of the neoplasm’s aggressivenes.
Thus cancers are classified as grade I to IV
with increasing neoplasia.

 The staging of cancers is based on the size of

the primary lesion, its extent of spread to
regional lymph nodes and the presence or
absence of blood, born metastasis.
 TNM system:
-T: for primary tumor.
-N: for regional lymph node involvement.
-M: for metastasis.
 A. Oncogen & protooncogen.
 Oncogen or cancer causing genes are derived
from protooncogens, cellular genes that
promote growth and differentiation.

 Protooncogen may become oncogenic by :

-Retroviral transduction (v-onc).
-or by influence that alter their behaviour in
situ, thereby converting them in to cellular
oncogens ( c-onc)
 Activation of protooncogen.
The specific lesion that lead to structural &
regularly change that affect protooncogen.
-point mutation.
-Chromosomal translocation.
-gene amplification.
 B. Cancer suppressor gene:
The lost of these gene is a key event in many
possibly all human tumors.

 C. Gene that regulate apoptosis.

Apoptosis is programmed cell death.
 A large number of agents cause genetic
damage and induce neoplastic transformation
of cells.

 A.Chemical carcinogenic:
E.g: alkilating agent, acylating agents,
nitrosamine, amides, vinylchlorides,
benzidine, hydrocarbon policyclic aromatic.
 B. Radiation carcinogen:
-Ultraviolet rays.
-Electromagnetic (x rays, gamma rays,
particulate alfa,beta, proton, netron.

 C.Viral carcinogen.
 1.DNA oncogenic viruses.
-Human papilloma virus (HPV).
Definitely cause benign squamous papiloma
also been implicated in genesis of several
cancer particulary squamous cell carcinoma
of the servix.
 -Epstein Barr Viruses (EBV).
Nasopharyngeal carcinoma & Burkitt’s
lymphoma tumor associated with EBV.

 Hepatitis B virus (HBV).

Hepatocellelar carcinoma.

 2.RNA oncogen viruses.

HTLV 1(human T cell leukemia virus type 1).
Associated with form of T cell
 1. Geographic & enviromental.
 The death rate for stomach carcinoma in both
males & females, seven to eight time in Japan
than in USA.
 Smoking particularly of cigarettes has been
implicated in cancer of the mouth, pharynx,
larynx, esophagus, pancreas & bladder.
 2. Age:
Most carcinoma occur in the later year of life
(55 year and over).
Common neoplasma of infancy:
Neuroblastoma, Wilm’ tumor, Retinoblastoma,
acut leukemia, Rhabdomyosarcoma.

 3.Heriditary:
Familial retinoblastoma, adenomatous polyp,
Breast cancer, ovarian cancer, colon cancer.
 4.Aquired preneoplastic disorders:
-About 80% of hepatocellular carcinoma arise
in cirrhotic liver.
-The chronic atrophic gastritis of pernicious
anemia, Solar keratosis of the skin, Chronic
ulcerative colitis, Leukoplakia of the oral
cavity, vulva & penis have association with
 1.Histologic methods
 2.Cytologic methods.
-Pap’s smear (papaniculauo smear).
-Fine needle aspiration biopsy (FNAB).
 3. Vries coop (VC).
 4. Imunohistochemistry.
The avaibility of specific monoclonal
antibodies has greatly facilitated the
identification of cell pruducts or surface
 5.Molecular diagnosis.
Flow cytometry.
 6.Tumor markers:
 -Carcinoembryonic antigen (CEA)
Significan elevetion in breast carcinoma,
colorectal CA, pancreatic CA, gastric CA.

Alpha fetoprotein (AFP).

Abnormal plasma elevation are encountered
in the liver & germ cell of testis/ovari. Also
elevated in: colon, lung, pancreas CA.
-PSA (prostat specific antigen)